Intraoperative hemodynamics and risk of cardiac surgery‐associated acute kidney injury: An observation study and a feasibility clinical trial

Author:

Noe Khin M.12,Don Andrea1,Cochrane Andrew D.23,Zhu Michael Z. L.123,Ngo Jennifer P.14ORCID,Smith Julian A.23,Thrift Amanda G.5,Vogiatjis Johnny1,Martin Andrew123,Bellomo Rinaldo6789,McMillan James10,Evans Roger G.128ORCID

Affiliation:

1. Cardiovascular Disease Program, Department of Physiology Biomedicine Discovery Institute, Monash University Melbourne Victoria Australia

2. Department of Surgery School of Clinical Sciences at Monash Health, Monash University Melbourne Victoria Australia

3. Department of Cardiothoracic Surgery Monash Health, Monash University Melbourne Victoria Australia

4. Department of Cardiac Physiology National Cerebral and Cardiovascular Center Research Institute Osaka Japan

5. Department of Medicine School of Clinical Sciences at Monash Health, Monash University Melbourne Victoria Australia

6. Department of Critical Care University of Melbourne Melbourne Victoria Australia

7. Department of Intensive Care, Austin Health Heidelberg Victoria Australia

8. Pre‐clinical Critical Care Unit Florey Institute of Neuroscience and Mental Health, University of Melbourne Melbourne Victoria Australia

9. Australian and New Zealand Intensive Care Research Centre Monash University Melbourne Victoria Australia

10. Perfusion Services Pty Ltd Melbourne Victoria Australia

Abstract

AbstractTargeting greater pump flow and mean arterial pressure (MAP) during cardiopulmonary bypass (CPB) could potentially alleviate renal hypoxia and reduce the risk of postoperative acute kidney injury (AKI). Therefore, in an observational study of 93 patients undergoing on‐pump cardiac surgery, we tested whether intraoperative hemodynamic management differed between patients who did and did not develop AKI. Then, in 20 patients, we assessed the feasibility of a larger‐scale trial in which patients would be randomized to greater than normal target pump flow and MAP, or usual care, during CPB. In the observational cohort, MAP during hypothermic CPB averaged 68.8 ± 8.0 mmHg (mean ± SD) in the 36 patients who developed AKI and 68.9 ± 6.3 mmHg in the 57 patients who did not (p = 0.98). Pump flow averaged 2.4 ± 0.2 L/min/m2 in both groups. In the feasibility clinical trial, compared with usual care, those randomized to increased target pump flow and MAP had greater mean pump flow (2.70 ± 0.23 vs. 2.42 ± 0.09 L/min/m2 during the period before rewarming) and systemic oxygen delivery (363 ± 60 vs. 281 ± 45 mL/min/m2). Target MAP ≥80 mmHg was achieved in 66.6% of patients in the intervention group but in only 27.3% of patients in the usual care group. Nevertheless, MAP during CPB did not differ significantly between the two groups. We conclude that little insight was gained from our observational study regarding the impact of variations in pump flow and MAP on the risk of AKI. However, a clinical trial to assess the effects of greater target pump flow and MAP on the risk of AKI appears feasible.

Funder

National Heart Foundation of Australia

Publisher

Wiley

Subject

Physiology (medical),Pharmacology,Physiology

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